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  1. Book ; Thesis: Produktion des Neurotrophins BDNF und Expression des BDNF-Rezeptors

    Gallmeier, Eike Meinfried Wilhelm

    TrkB durch humane Immunzellen

    2001  

    Author's details vorgelegt von Eike Meinfried Wilhelm Gallmeier
    Language German
    Size 89 S., graph. Darst., 21 cm
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis München, Univ., Diss., 2001
    HBZ-ID HT013272427
    Database Catalogue ZB MED Medicine, Health

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  2. Book ; Online ; Thesis: Synthetic lethal interactions between ATR and DNA polymerases as a novel concept for individualized cancer therapy

    Job, Albert [Verfasser] / Gallmeier, Eike [Akademischer Betreuer]

    2019  

    Author's details Albert Job ; Betreuer: Eike Gallmeier
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language English
    Publisher Philipps-Universität Marburg
    Publishing place Marburg
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  3. Article ; Online: Controversy on the time to progression of pancreatic ductal adenocarcinoma.

    Gallmeier, Eike / Hernaez, Ruben / Gress, Thomas M

    Gut

    2015  Volume 64, Issue 11, Page(s) 1676–1677

    MeSH term(s) Adenocarcinoma/pathology ; Carcinoma, Pancreatic Ductal/pathology ; Female ; Humans ; Male ; Pancreatic Neoplasms/pathology
    Language English
    Publishing date 2015-11
    Publishing country England
    Document type Comment ; Journal Article
    ZDB-ID 80128-8
    ISSN 1468-3288 ; 0017-5749
    ISSN (online) 1468-3288
    ISSN 0017-5749
    DOI 10.1136/gutjnl-2014-309066
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Book ; Online ; Thesis: Einfluss der qualitativen und quantitativen HSP27-Expression auf die in vitro Chemo- und Radiosensitivität von Pankreaskarzinomzellen

    Buchner, Denise / Gallmeier, Eike

    2014  

    Author's details Denise Buchner. Betreuer: Eike Gallmeier
    Language German
    Size Online-Ressource
    Publisher Universitätsbibliothek der Ludwig-Maximilians-Universität
    Publishing place München
    Document type Book ; Online ; Thesis
    Thesis / German Habilitation thesis München, Ludwig-Maximilians-Universität, Diss., 2014
    Database Former special subject collection: coastal and deep sea fishing

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  5. Article ; Online: Functional evaluation of variants of unknown significance in the BRCA2 gene identified in genetic testing.

    Heczkova, Marie / Machackova, Eva / Macinga, Peter / Gallmeier, Eike / Cahova, Monika / Spicak, Julius / Jirsa, Milan / Foretova, Lenka / Hucl, Tomas

    Cancer biology & therapy

    2019  Volume 20, Issue 5, Page(s) 633–641

    Abstract: Heterozygous germline BRCA2 mutations predispose to breast, ovarian, pancreatic and other types of cancer. The presence of a pathogenic mutation in patients or their family members warrants close surveillance or prophylactic surgery. Besides clearly ... ...

    Abstract Heterozygous germline BRCA2 mutations predispose to breast, ovarian, pancreatic and other types of cancer. The presence of a pathogenic mutation in patients or their family members warrants close surveillance or prophylactic surgery. Besides clearly pathogenic mutations, variants leading only to a single amino acid substitution are often identified. The influence of such variants on cancer risk is often unknown, making their presence a major clinical problem. When genetic methods are insufficient to classify these variants, functional assays with various cellular models are performed. We developed and applied a new syngeneic model of human cancer cells to test all variants of unknown significance in exon 18 identified by genetic testing of high-risk cancer patients in the Czech Republic, via introduction of constructs containing each of these variants into the wild-type allele of BRCA2-heterozygous DLD1 cells (BRCA2
    MeSH term(s) Adult ; Aged ; BRCA2 Protein/genetics ; Cell Line, Tumor ; Czech Republic ; DNA Mutational Analysis/methods ; Exons/genetics ; Feasibility Studies ; Female ; Genetic Predisposition to Disease ; Genetic Testing/methods ; Humans ; Male ; Markov Chains ; Medical History Taking ; Middle Aged ; Models, Biological ; Mutation ; Neoplasms/diagnosis ; Neoplasms/genetics ; Risk Assessment/methods
    Chemical Substances BRCA2 Protein ; BRCA2 protein, human
    Language English
    Publishing date 2019-01-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2146305-0
    ISSN 1555-8576 ; 1538-4047
    ISSN (online) 1555-8576
    ISSN 1538-4047
    DOI 10.1080/15384047.2018.1550566
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Book ; Online ; Thesis: Einfluss der qualitativen und quantitativen HSP27-Expression auf die in vitro Chemo- und Radiosensitivität von Pankreaskarzinomzellen

    Buchner, Denise [Verfasser] / Gallmeier, Eike [Akademischer Betreuer]

    2014  

    Author's details Denise Buchner. Betreuer: Eike Gallmeier
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Publisher Universitätsbibliothek der Ludwig-Maximilians-Universität
    Publishing place München
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  7. Article ; Online: The POLD1

    Job, Albert / Tatura, Marina / Schäfer, Cora / Lutz, Veronika / Schneider, Hanna / Lankat-Buttgereit, Brigitte / Zielinski, Alexandra / Borgmann, Kerstin / Bauer, Christian / Gress, Thomas M / Buchholz, Malte / Gallmeier, Eike

    Scientific reports

    2020  Volume 10, Issue 1, Page(s) 18924

    Abstract: Inhibition of the kinase ATR, a central regulator of the DNA damage response, eliminates subsets of cancer cells in certain tumors. As previously shown, this is at least partly attributable to synthetic lethal interactions between ATR and POLD1, the ... ...

    Abstract Inhibition of the kinase ATR, a central regulator of the DNA damage response, eliminates subsets of cancer cells in certain tumors. As previously shown, this is at least partly attributable to synthetic lethal interactions between ATR and POLD1, the catalytic subunit of the polymerase δ. Various POLD1 variants have been found in colorectal cancer, but their significance as therapeutic targets for ATR pathway inhibition remains unknown. Using CRISPR/Cas9 in the colorectal cancer cell line DLD-1, which harbors four POLD1 variants, we established heterozygous POLD1-knockout clones with exclusive expression of distinct variants to determine the functional relevance of these variants individually by assessing their impact on ATR pathway activation, DNA replication, and cellular sensitivity to inhibition of ATR or its effector kinase CHK1. Of the four variants analyzed, only POLD1
    MeSH term(s) Amino Acid Substitution ; Animals ; CRISPR-Cas Systems ; Cell Line, Tumor ; Cell Survival/drug effects ; Checkpoint Kinase 1/antagonists & inhibitors ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; DNA Polymerase III/genetics ; DNA Replication/drug effects ; Gene Knockout Techniques ; Humans ; Mice ; Pyrimidines/administration & dosage ; Pyrimidines/pharmacology ; Sulfoxides/administration & dosage ; Sulfoxides/pharmacology ; Xenograft Model Antitumor Assays
    Chemical Substances Pyrimidines ; Sulfoxides ; ceralasertib (85RE35306Z) ; CHEK1 protein, human (EC 2.7.11.1) ; Checkpoint Kinase 1 (EC 2.7.11.1) ; POLD1 protein, human (EC 2.7.7.-) ; DNA Polymerase III (EC 2.7.7.7)
    Language English
    Publishing date 2020-11-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-020-76033-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Supraclavicular approach for central venous catheterization: "safer, simpler, speedier".

    Cunningham, Steven C / Gallmeier, Eike

    Journal of the American College of Surgeons

    2007  Volume 205, Issue 3, Page(s) 514–6; author reply 516–7

    MeSH term(s) Catheterization, Central Venous/adverse effects ; Catheterization, Central Venous/methods ; Catheters, Indwelling/adverse effects ; Clavicle ; Device Removal/adverse effects ; Humans ; Jugular Veins ; Randomized Controlled Trials as Topic ; Subclavian Vein
    Language English
    Publishing date 2007-09
    Publishing country United States
    Document type Comment ; Letter
    ZDB-ID 1181115-8
    ISSN 1879-1190 ; 1072-7515
    ISSN (online) 1879-1190
    ISSN 1072-7515
    DOI 10.1016/j.jamcollsurg.2007.05.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Inactivation of PRIM1 Function Sensitizes Cancer Cells to ATR and CHK1 Inhibitors.

    Job, Albert / Schmitt, Lisa-Maria / von Wenserski, Lisa / Lankat-Buttgereit, Brigitte / Gress, Thomas M / Buchholz, Malte / Gallmeier, Eike

    Neoplasia (New York, N.Y.)

    2018  Volume 20, Issue 11, Page(s) 1135–1143

    Abstract: The phosphoinositide 3-kinase-related kinase ATR is a central regulator of the DNA damage response. Its chemical inhibition eliminates subsets of cancer cells in various tumor types. This effect is caused at least partly by the synthetically lethal ... ...

    Abstract The phosphoinositide 3-kinase-related kinase ATR is a central regulator of the DNA damage response. Its chemical inhibition eliminates subsets of cancer cells in various tumor types. This effect is caused at least partly by the synthetically lethal relationship between ATR and certain DNA repair genes. In a previous screen using an siRNA library against DNA repair genes, we identified PRIM1, a part of the polymerase α-primase complex, as acting synthetically lethal with ATR. Applying a genetic ATR knock-in model of colorectal cancer cells, we confirmed that PRIM1 depletion inhibited proliferation of ATR-deficient cells and excluded artifacts due to clonal variation using an ATR reexpressing cell clone. We expanded these data by demonstrating in different cell lines that also chemical inhibition of ATR or its main effector kinase CHK1 reduces proliferation upon depletion of PRIM1. Mechanistically, PRIM1 depletion in ATR-deficient cells caused S-phase stasis in the absence of increased DNA damage followed by Wee1-mediated activation of caspase 8 and apoptosis. As PRIM1 inactivation sensitizes cancer cells to ATR and CHK1 inhibitors, mutations in PRIM1 or other components of the polymerase α-primase complex could represent novel targets for individualized tumor therapeutic approaches using ATR/CHK1 inhibitors, as has been previously demonstrated for POLD1, the catalytic subunit of polymerase δ.
    MeSH term(s) Apoptosis/drug effects ; Apoptosis/genetics ; Ataxia Telangiectasia Mutated Proteins/antagonists & inhibitors ; Ataxia Telangiectasia Mutated Proteins/genetics ; Cell Cycle/drug effects ; Cell Cycle/genetics ; Cell Line, Tumor ; Cell Proliferation ; Checkpoint Kinase 1/antagonists & inhibitors ; DNA Primase/antagonists & inhibitors ; Drug Resistance, Neoplasm ; Gene Expression ; Histones/metabolism ; Humans ; Protein Kinase Inhibitors/pharmacology ; RNA Interference ; RNA, Small Interfering/genetics ; Synthetic Lethal Mutations
    Chemical Substances Histones ; Protein Kinase Inhibitors ; RNA, Small Interfering ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Checkpoint Kinase 1 (EC 2.7.11.1) ; DNA Primase (EC 2.7.7.-) ; PRIM1 protein, human (EC 2.7.7.-)
    Language English
    Publishing date 2018-09-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1483840-0
    ISSN 1476-5586 ; 1522-8002
    ISSN (online) 1476-5586
    ISSN 1522-8002
    DOI 10.1016/j.neo.2018.08.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: MKK4 as oncogene or tumor suppressor: in cancer and senescence, the story's getting old.

    Cunningham, Steven C / Gallmeier, Eike / Kern, Scott E

    Aging

    2010  Volume 2, Issue 11, Page(s) 752–753

    MeSH term(s) Animals ; Cellular Senescence/physiology ; Genes, Tumor Suppressor ; Humans ; MAP Kinase Kinase 4/genetics ; MAP Kinase Kinase 4/metabolism ; Neoplasms/enzymology ; Neoplasms/genetics ; Oncogenes
    Chemical Substances MAP Kinase Kinase 4 (EC 2.7.12.2) ; MAP2K4 protein, human (EC 2.7.12.2)
    Language English
    Publishing date 2010-11-17
    Publishing country United States
    Document type Journal Article
    ISSN 1945-4589
    ISSN (online) 1945-4589
    DOI 10.18632/aging.100233
    Database MEDical Literature Analysis and Retrieval System OnLINE

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